Glucose transport occurs in the adipose cell through a highly specific facilitated diffusion process. Insulin, in turn, increases the maximum transport velocity. A specific D-glucose inhibitable 3H-cytochalasin B binding assay has recently been used to quantitate the number of glucose transport systems in the purified plasma membranes of isolated rat adipose cells and to demonstrate that insulin stimulates glucose transport primarily by increasing the number of functional glucose transport systems. This assay has now been further used to identify a high specific activity intracellular pool of transport systems which sediments with the Golgi fraction during differential ultracentrifugation. Insulin, in turn, stoichiometrically decreases the number of transport systems in this pool at the same time that it increases their number in the plasma membranes. These effects of insulin are rapid, correlating in time with insulin's stimulatory action on glucose transport itself in the intact cell, and completely reversible by treating the insulin-stimulated cell with excess insulin antibody, suggesting a translocation process. Preliminary results suggest that insulin may stimulate glucose transport in the rat diaphragm in vitro by the same mechanism.